Acute Myocardial Infarction, AMI or ‘Heart Attack"January 2, 2010 | 12:43 pm | Cardiology | One Comment
Acute Myocardial Infarction
Myocardial infarction (MI) or acute myocardial infarction (AMI), is the interruption of blood supply to part of the heart, causing heart cells to die, commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids and white blood cells in the wall of an artery.
The resulting ischemia and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).
- Pain is the cardinal symptom. Chest pain is often described as tightness, heaviness, crushing or squeezing in the chest. It is retrosternal and often radiates down the left arm , neck, epigastrium or back and sometimes the jaw , usually more severe and lasts longer than angina. Painless MI is seen in older and diabetic patients.
- Diaphoretic, pale ,cool moist skin, anxiety and fear of impending death.
- Nausea and vomiting common in inferior wall MI
- Collapse and syncope due to arrhythmia or profound hypotension.
Signs of sympathetic activation- pallor, sweating, tachycardia
Signs of vagal activation- vomiting, bradycardia
Signs of impaired myocardial function- hypotension, oliguria, cold peripheries narrow pulse pressure raised jugular venous pressure (right ventricular infarct) third heart sound quiet first heart sound ,diffuse apical impulse lung crepitations.
Signs of tissue damage- fever
Signs of complication- mitral regurgitation, pericarditis
ECG-the earliest sign is usually ST elevation (appears within minutes)
Progressive loss of R wave , developing Q wave, resolution of ST elevation and terminal T wave inversion.(within hrs)
Deep Q wave and T wave inversion.(within days)
Old or established infarct pattern; Q wave tends to persist but the T wave changes become less marked.(after several weeks or months)
a) Transmural (Q wave) MI
-presence of ST elevation with subsequent development of pathologic Q waves.
Pathologic Q waves have a width of 0.04 seconds or more and an amplitude >=25% of the R wave in that lead.
MI can be classified based on the location of the Q waves:
Inferior MI:Q waves in II, III, aVF
High lateral MI:Q waves in I,Avl
Anteroseptal MI: Q waves in V1 through V3
Anteroseptal MI: Q waves in V4 through V6
Localized anterior MI:Q waves in V2 through V4
Anterior MI: Q waves in V1 through V6, I,aVL
Right ventricular MI:Q waves in V4 and V5
Posterior wall MI: large R in both V1 and V2 and Q in V6
b) Non Q wave MI:
involves subendocardial zone of left ventricle
does not exhibit any abnormal Q waves or ST elevation
exhibits marked ST segment depression of 1mm or more resulting in either horizontal or down-sloping ST segments in all precordial leads.
Enzyme Rise(hrs) Peak(hrs) Return to baseline(days)
troponin 3-6 12-24 7-10
CK-MB 4-6 12-36 3-4
LD 12 24-48 10-14
Other blood tests: leucocytosis, ESR raised C-reactive protein raised
Chest X-ray: demonstrate pulmonary edema , cardiomegaly due to pre-existing myocardial damage.
Echocardiography: assessing left and right ventricular function and detecting important complications such as mural thrombus, cardiac rupture, VSD, mitral regurgitation and pericardial effusion.
1) Medical therapy
a) IV-O2 monitor
b) NTG-0.4 mg sublingually repeated every 2-5 minutes upto 3 times, if no relief use 5-10mg/min IV at 2-5 min intervals to a max. of 100mg/min
c) Aspirin : 160- 300mg PO preferably chewed
d) B blockers- cardioselective (B1 ) blockers
metoprolol:5-15mg IV over 5min
atenolol: 5-10 mg IV over 5min
e) Morphine: 2 mg IV bolus every 5 minutes titrated to effect
f) Magnesium: def. produce cardiac arrhythmias , secondary hypokalemia . 1-2g IV over 10-20 minutes followed by continuous infusion 1-2g/h
g) Thrombolytics: streptokinase, urokinase, anisoylated plasminogen streptokinase activator complex(APSAC, anistreplase), alteplase, retaplase.
-Acute MI by ECG criteria of >0.1mV ST segment elevation in at least two contiguous leads or new left bundle branch block
-Absence of cardiogenic shock.
Administered in<6hrs most beneficial.
(note:-Thrombolytics are used in TT of MI but not unstable Angina)
h) arterial vasodilators:- are used in left and right ventricle infarct.
i) GP IIb-IIIa receptor inhibitors: used for non Q wave MI
j) Subcutaneous heparin(12,500U twice daily), given in addition to oral aspirin, may prevent reinfarction after successful thrombolysis and reduce risk of thromboembolic complications.
2) Surgical therapy
a)Percutaneous coronary transluminal angioplasty (PTCA)
b)Coronary artery bypass grafting (CABG)
|EARLY MANAGEMENT OF ACUTE MI|
|Provide facilities for defibrillation|
-High flow oxygen -IV analgesia
-IV access -Aspirin 300 mg
Primary PCI or thrombolysis
Tags: AMI, heart attack, MI, myocardial infarction
Last updated: August 17, 2010